Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/10183
Title: The sympathoinhibitory effects of systemic cholecystokinin are dependent on neurons in the caudal ventrolateral medulla in the rat.
Authors: Sartor, Daniela M;Verberne, Anthony J M
Affiliation: dsartor@unimelb.edu.au
University of Melbourne, Clinical Pharmacology and Therapeutics Unit, Dept. of Medicine, Austin Health, Heidelberg, Victoria 3084, Australia
Issue Date: 22-Jun-2006
Citation: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology 2006; 291(5): R1390-8
Abstract: The gastrointestinal hormone CCK inhibits a subset of presympathetic neurons in the rostroventrolateral medulla (RVLM) that may be responsible for driving the sympathetic vasomotor outflow to the gastrointestinal circulation. We tested the hypothesis that the central neurocircuitry of this novel sympathoinhibitory reflex involves a relay in the caudal ventrolateral medullary (CVLM) depressor area. Blood pressure and greater splanchnic sympathetic nerve discharge (SSND) or lumbar sympathetic nerve discharge (LSND) were monitored in anesthetised, paralyzed male Sprague-Dawley rats. The effects of phenylephrine (PE, 10 microg/kg iv; baroreflex activation), phenylbiguanide (PBG, 10 microg/kg iv; von Bezold-Jarisch reflex) and CCK (4 or 8 microg/kg iv) on SSND or LSND, were tested before and after bilateral injection of 50-100 nl of the GABAA agonist muscimol (1.75 mM; n=6, SSND; n=7, LSND) or the excitatory amino acid antagonist kynurenate (55 mM; n=7, SSND) into the CVLM. PE and PBG elicited splanchnic and lumbar sympathoinhibitory responses that were abolished by bilateral muscimol or kynurenate injection into the CVLM. Similarly, the inhibitory effect of CCK on SSND was abolished after neuronal inhibition within the CVLM. In contrast, CCK-evoked lumbar sympathoexcitation was accentuated following bilateral CVLM inhibition. In control experiments (n=7), these agents were injected outside the CVLM and had no effect on splanchnic sympathoinhibitory responses to PE, PBG, and CCK. In conclusion, neurons in the CVLM are necessary for the splanchnic but not lumbar sympathetic vasomotor reflex response to CCK. This strengthens the view that subpopulations of RVLM neurons supply sympathetic vasomotor outflow to specific vascular territories.
Internal ID Number: 16793934
URI: http://ahro.austin.org.au/austinjspui/handle/1/10183
DOI: 10.1152/ajpregu.00314.2006
URL: http://www.ncbi.nlm.nih.gov/pubmed/16793934
Type: Journal Article
Subjects: Adrenergic alpha-Agonists.pharmacology
Animals
Biguanides.pharmacology
Cholagogues and Choleretics.pharmacology
Cholecystokinin.pharmacology
Excitatory Amino Acid Antagonists.pharmacology
GABA Agonists.pharmacology
Kynurenic Acid.pharmacology
Lumbosacral Plexus.drug effects.physiology
Male
Medulla Oblongata.drug effects.physiology
Muscimol.pharmacology
Neurons.drug effects.physiology
Phenylephrine.pharmacology
Rats
Rats, Sprague-Dawley
Serotonin Receptor Agonists.pharmacology
Splanchnic Nerves.drug effects.physiology
Sympathetic Nervous System.drug effects.physiology
Synaptic Transmission.drug effects.physiology
Appears in Collections:Journal articles

Files in This Item:
There are no files associated with this item.


Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.